IE63-specific T-cell responses associate with control of subclinical varicella zoster virus reactivation in individuals with malignancies

Abstract

Background: Reactivation of the varicella zoster virus (VZV) is more common in patients with malignancies; however, the molecular and cellular mechanisms underlying this susceptibility are unclear.

Methods: Using ex vivo interferon-gamma ELISpot assays, we set out to analyse VZV-specific immune responses in a large cohort of patients with malignancies.

Results: We observed that patients with malignancies had impaired VZV-specific T-cell responses, particularly in those with haematological malignancies and breast carcinoma. Immediate-early protein 63 (IE63)-specific T-cell responses were significantly impaired in those with subclinical VZV re-activation.

Conclusions: Our results suggest that T-cell responses to IE63 are important in controlling VZV replication.

Figure 1

Ex vivo IFNγ ELISpot responses to VZV live attenuated vaccine, overlapping gE 20-mer peptide pool and overlapping IE63 20-mer peptide pools in patients with malignancies and healthy seropositive volunteers with no evidence of VZV reactivation.

Figure 2

Ex vivo IFNγ ELISpot responses to VZV live attenuated vaccine, overlapping gE 20-mer peptide pool and overlapping IE63 20-mer peptide pool in patients with haematological and solid malignancies. The error bars represent the s.e.m.

Figure 3

Ex vivo IFNγ ELISpot responses to VZV live attenuated vaccine (VZV), overlapping gE 20-mer peptide pool and overlapping IE63 20-mer peptide pool in patients with malignancies who had subclinical VZV viraemia and those who were non-viraemic.